Cell Signaling Technology
XP Monoclonal Antibody

Product Pathways - Chromatin Regulation / Epigenetics

HMGA1 (D6A4) XP® Rabbit mAb #7777

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-IC H Mk (B) Endogenous 18 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  Mk=Monkey  B=Bovine
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

HMGA1 (D6A4) XP® Rabbit mAb recognizes endogenous levels of total HMGA1 protein, isoforms 1a and 1b. Based on sequence homology, this antibody is not predicted to cross-react with HMGA2.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly68 of human HMGA1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using HMGA1 (D6A4) XP® Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).

IP

IP

Immunoprecipitation of HMGA1 from COS-7 cell extracts, using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 3) or HMGA1 (D6A4) XP® Rabbit mAb (lane 2). Lane 1 is 10% input. Western blot analysis was performed using HMGA1 (D6A4) XP® Rabbit mAb.

IF-IC

IF-IC

Confocal immunofluorescent analysis of NCCIT (high expression; left) or MCF7 (low expression; right) cells, using HMGA1 (D6A4) XP® Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).


Background

HMGA1, formerly known as HMG-I/Y, belongs to a family of high mobility group proteins that contain an AT-hook DNA binding domain. HMGA proteins are considered architectural transcription factors; they do not have direct transcriptional activation capacity, but instead regulate gene expression by changing DNA conformation through binding to AT-rich regions in the DNA and/or direct interaction with other transcription factors (1,2). HMGA1 is highly expressed during embryogenesis and in embryonic stem cells, but not in fully differentiated adult tissues (2-4). Research studies have shown that HMGA1 is over-expressed in rapidly dividing neoplastic cells and a wide variety of aggressive cancers, including thyroid, colon, breast, pancreas, and prostate (2-4). Investigators have shown that forced expression of HMGA1 induces cellular transformation and an epithelial-to-mesenchymal transition (EMT), while inhibition of HMGA1 expression blocks anchorage-independent cell growth and proliferation of cancer cells, suggesting that HMGA1 contributes to carcinogenesis by inducing and maintaining a de-differentiated, highly proliferative cell state (5-8).

  1. Cleynen, I. and Van de Ven, W.J. (2008) Int J Oncol 32, 289-305.
  2. Resar, L.M. (2010) Cancer Res 70, 436-9.
  3. Chiappetta, G. et al. (1996) Oncogene 13, 2439-46.
  4. Ben-Porath, I. et al. (2008) Nat Genet 40, 499-507.
  5. Wood, L.J. et al. (2000) Mol Cell Biol 20, 5490-502.
  6. Wood, L.J. et al. (2000) Cancer Res 60, 4256-61.
  7. Xu, Y. et al. (2004) Cancer Res 64, 3371-5.
  8. Scala, S. et al. (2000) Proc Natl Acad Sci U S A 97, 4256-61.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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